How much is too much? Phenotypic consequences of Rai1 overexpression in mice. - Wikidata - wikimedia - TriplyDB

How much is too much? Phenotypic consequences of Rai1 overexpression in mice.

How much is too much? Phenotypic consequences of Rai1 overexpression in mice.

http://www.wikidata.org/entity/Q44936179

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Phenotypic consequences of copy number variation: insights from Smith-Magenis and Potocki-Lupski syndrome mouse models A duplication CNV that conveys traits reciprocal to metabolic syndrome and protects against diet-induced obesity in mice and men Cerebellar zonal patterning relies on Purkinje cell neurotransmission.Dietary regimens modify early onset of obesity in mice haploinsufficient for Rai1.Retinoic Acid Induced 1, RAI1: A Dosage Sensitive Gene Related to Neurobehavioral Alterations Including Autistic Behavior Mouse models of genomic syndromes as tools for understanding the basis of complex traits: an example with the smith-magenis and the potocki-lupski syndromes Behavioral characterization of mouse models of neuroferritinopathy.Identifying the primary site of pathogenesis in amyotrophic lateral sclerosis - vulnerability of lower motor neurons to proximal excitotoxicity.Genomic sister-disorders of neurodevelopment: an evolutionary approach Evidence for genetic regulation of mRNA expression of the dosage-sensitive gene retinoic acid induced-1 (RAI1) in human brain Failure of neuronal homeostasis results in common neuropsychiatric phenotypes.Smith-Magenis syndrome: haploinsufficiency of RAI1 results in altered gene regulation in neurological and metabolic pathways.Genetic architecture of reciprocal CNVs.Gene discovery and functional assessment of rare copy-number variants in neurodevelopmental disorders.Yin-yang actions of histone methylation regulatory complexes in the brain.Molecular and Neural Functions of Rai1, the Causal Gene for Smith-Magenis Syndrome.Rai1 haploinsufficiency causes reduced Bdnf expression resulting in hyperphagia, obesity and altered fat distribution in mice and humans with no evidence of metabolic syndrome.RAI1 Overexpression Promotes Altered Circadian Gene Expression and Dyssomnia in Potocki-Lupski Syndrome.Multi-ethnic Meta-analysis Identifies RAI1 as a Possible Obstructive Sleep Apnea Related Quantitative Trait Locus in Men.Cerebellar granule cell replenishment postinjury by adaptive reprogramming of Nestin+ progenitors.Applying chlorogenic acid in an alginate scaffold of chondrocytes can improve the repair of damaged articular cartilage.

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P2860

How much is too much? Phenotypic consequences of Rai1 overexpression in mice.

http://www.wikidata.org/entity/Q44936179

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2008 nî lūn-bûn

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2008年の論文

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2008年学术文章

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2008年学术文章

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2008年学术文章

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2008年学术文章

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2008年学术文章

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2008年學術文章

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2008年學術文章

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2008年學術文章

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name

How much is too much? Phenotypic consequences of Rai1 overexpression in mice.

@en

How much is too much? Phenotypic consequences of Rai1 overexpression in mice.

@nl

type

label

How much is too much? Phenotypic consequences of Rai1 overexpression in mice.

@en

How much is too much? Phenotypic consequences of Rai1 overexpression in mice.

@nl

prefLabel

How much is too much? Phenotypic consequences of Rai1 overexpression in mice.

@en

How much is too much? Phenotypic consequences of Rai1 overexpression in mice.

@nl

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European Journal of Human Genetics

P1476

How much is too much? Phenotypic consequences of Rai1 overexpression in mice.

@en

P2093

Maja Bucan

http://www.w3.org/2001/XMLSchema#string

Mary E Tokarz

http://www.w3.org/2001/XMLSchema#string

Nisha Patel

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Rebecca E Slager

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Santhosh Girirajan

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Sarah H Elsea

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P2860

Sensory ataxia and muscle spindle agenesis in mice lacking the transcription factor Egr3

Genes in a refined Smith-Magenis syndrome critical deletion interval on chromosome 17p11.2 and the syntenic region of the mouse

Rai1 duplication causes physical and behavioral phenotypes in a mouse model of dup(17)(p11.2p11.2).

Characterization of Potocki-Lupski syndrome (dup(17)(p11.2p11.2)) and delineation of a dosage-sensitive critical interval that can convey an autism phenotype

Chondrodysplasia and neurological abnormalities in ATF-2-deficient mice

Interstitial deletion of (17)(p11.2p11.2) in nine patients

A targeted mutation of the D3 dopamine receptor gene is associated with hyperactivity in mice

Inactivation of Rai1 in mice recapitulates phenotypes observed in chromosome engineered mouse models for Smith-Magenis syndrome

In vivo response to high-resolution variation of Tbx1 mRNA dosage

Social interaction and sensorimotor gating abnormalities in mice lacking Dvl1

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941-954

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10.1038/EJHG.2008.21

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8

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16

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5565874

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1033444626

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